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- Publisher Website: 10.1039/C8FO02315H
- Scopus: eid_2-s2.0-85066134142
- PMID: 31038133
- WOS: WOS:000469145900038
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Article: Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1 phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells
Title | Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1 phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells |
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Authors | |
Keywords | Cell death Cell membranes Diseases Lipids |
Issue Date | 2019 |
Publisher | Royal Society of Chemistry. The Journal's web site is located at http://pubs.rsc.org/en/journals/journalissues/fo |
Citation | Food & Function, 2019, v. 10 n. 5, p. 2729-2738 How to Cite? |
Abstract | Brosimone I is an isoprenoid-substituted flavonoid from Artocarpus heterophyllus. Here, we reported for the first time that brosimone I induced cell cycle G1 phase arrest and apoptosis in HCT116 human colon cancer cells. Brosimone I treatment increased the cytosolic Ca2+ level, and subsequently activated the CaMKKβ-AMPK pathway. STO-609, a CaMKKβ inhibitor, and compound C, an AMPK-specific inhibitor, attenuated brosimone I-induced loss of cell viability in HCT116 cells. Furthermore, brosimone I enhanced ER stress. Salubrinal, an ER stress inhibitor, reduced brosimone I-induced cell growth inhibition. In addition, brosimone I was found to increase ROS generation and the inhibition of ROS formation by NAC, a ROS inhibitor, attenuated brosimone I-induced cell death, cytosolic Ca2+ increase, and ER stress markers. Collectively, our findings reveal that brosimone I induces cell cycle G1 phase arrest and apoptosis via the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKKβ-AMPK signaling pathway. |
Persistent Identifier | http://hdl.handle.net/10722/276106 |
ISSN | 2023 Impact Factor: 5.1 2023 SCImago Journal Rankings: 1.073 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | ZHAO, Y | - |
dc.contributor.author | ZHOU, Y | - |
dc.contributor.author | Wang, M | - |
dc.date.accessioned | 2019-09-10T02:56:04Z | - |
dc.date.available | 2019-09-10T02:56:04Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Food & Function, 2019, v. 10 n. 5, p. 2729-2738 | - |
dc.identifier.issn | 2042-6496 | - |
dc.identifier.uri | http://hdl.handle.net/10722/276106 | - |
dc.description.abstract | Brosimone I is an isoprenoid-substituted flavonoid from Artocarpus heterophyllus. Here, we reported for the first time that brosimone I induced cell cycle G1 phase arrest and apoptosis in HCT116 human colon cancer cells. Brosimone I treatment increased the cytosolic Ca2+ level, and subsequently activated the CaMKKβ-AMPK pathway. STO-609, a CaMKKβ inhibitor, and compound C, an AMPK-specific inhibitor, attenuated brosimone I-induced loss of cell viability in HCT116 cells. Furthermore, brosimone I enhanced ER stress. Salubrinal, an ER stress inhibitor, reduced brosimone I-induced cell growth inhibition. In addition, brosimone I was found to increase ROS generation and the inhibition of ROS formation by NAC, a ROS inhibitor, attenuated brosimone I-induced cell death, cytosolic Ca2+ increase, and ER stress markers. Collectively, our findings reveal that brosimone I induces cell cycle G1 phase arrest and apoptosis via the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKKβ-AMPK signaling pathway. | - |
dc.language | eng | - |
dc.publisher | Royal Society of Chemistry. The Journal's web site is located at http://pubs.rsc.org/en/journals/journalissues/fo | - |
dc.relation.ispartof | Food & Function | - |
dc.subject | Cell death | - |
dc.subject | Cell membranes | - |
dc.subject | Diseases | - |
dc.subject | Lipids | - |
dc.title | Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle G1 phase arrest and apoptosis through ROS-dependent endoplasmic reticulum stress in HCT116 human colon cancer cells | - |
dc.type | Article | - |
dc.identifier.email | Wang, M: mfwang@hku.hk | - |
dc.identifier.authority | Wang, M=rp00800 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1039/C8FO02315H | - |
dc.identifier.pmid | 31038133 | - |
dc.identifier.scopus | eid_2-s2.0-85066134142 | - |
dc.identifier.hkuros | 303486 | - |
dc.identifier.volume | 10 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 2729 | - |
dc.identifier.epage | 2738 | - |
dc.identifier.isi | WOS:000469145900038 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 2042-6496 | - |